Effect of work rate on the functional ‘gain’ of Phase II pulmonary O2 uptake response to exercise

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Abstract

It has recently been reported that the ‘gain’ of Phase II increase in pulmonary oxygen uptake (i.e. the ‘fundamental’ increase in V̇O2 per unit increase in work rate; Gp) does not attain the anticipated value of ∼10 ml min−1 W−1 following the onset of high-intensity exercise. In the present study, we hypothesised that Gp would fall significantly below 10 ml min−1 W−1 only when the work rate exceeded the so-called ‘critical power’ (CP). Seven healthy males completed several ‘square-wave’ transitions from ‘unloaded’ cycling to work rates requiring 60 and 90% of the gas exchange threshold (GET), 40 and 80% of the difference between the GET and V̇O2 peak (i.e. below and above the CP, respectively), and 100, 110 and 120% of V̇O2 peak. Pulmonary V̇O2 was measured breath-by-breath and V̇O2 kinetics were determined using non-linear regression techniques. The asymptotic Gp was significantly lower at work rates above (7.2–8.6 ml min−1 W−1) compared to work rates below (9.3–9.7 ml min−1 W−1) the CP (P < 0.05). We conclude that the gain of Phase II increase in V̇O2 becomes significantly reduced when the work rate exceeds the CP.

Introduction

The dynamics of the pulmonary oxygen uptake (V̇O2) response upon the sudden transition from rest or very light exercise to constant work rate exercise of moderate intensity (i.e. below the gas exchange threshold, GET) and heavy and severe intensity (i.e. above the GET but below the V̇O2 peak) have been well characterised (Whipp and Wasserman, 1972, Linnarsson, 1974, Whipp et al., 1982, Whipp et al., 1982, Barstow and Mole, 1991, Paterson and Whipp, 1991, Ozyener et al., 2001). After a short time delay (∼15 s; Phase I), representing the increase in blood returned to the lungs from the action of the muscle pump and the immediate increase in cardiac output at exercise onset, V̇O2 rises in an exponential fashion with a time constant of ∼15–30 s (Phase II) towards the actual or initially-anticipated steady state V̇O2 required for the work rate. Phase II V̇O2 response projects towards an amplitude that has a gain (i.e. increase in V̇O2 above baseline per unit increase in external work rate above baseline; ΔV̇O2/ΔWR) approximating 10 ml min−1 W−1 (Whipp and Mahler, 1980, Roston et al., 1987, Barstow and Mole, 1991, Paterson and Whipp, 1991). For work rates above the GET, a second more slowly developing component of V̇O2 becomes evident after ∼2 min (Whipp and Wasserman, 1972). This V̇O2 ‘slow component’ is superimposed on the fundamental response and causes V̇O2 to rise above the expected value for the work rate (Linnarsson, 1974, Whipp and Mahler, 1980, Roston et al., 1987, Barstow and Mole, 1991, Paterson and Whipp, 1991).

The so-called ‘critical power’ (CP; Monod and Scherrer, 1965, Moritani et al., 1981), which represents the asymptote of the hyperbolic relationship between work rate and time to fatigue for an individual subject, demarcates the boundary between the heavy and severe exercise intensity domains (Whipp and Ward, 1990, Hill et al., 2002). If the exercise work rate is in the heavy domain, then a delayed (and elevated) steady state in V̇O2 is ultimately established whereas if the work rate is in the severe domain, V̇O2 will continue to rise with time until the exercise is terminated or V̇O2 peak is attained (Poole et al., 1988). Exercise in the heavy domain is associated with a mild but stable metabolic (lactic) acidosis (typically 2–4 mM whole blood [lactate]) whereas exercise is the severe domain is associated with a substantial and progressively increasing lactic acidosis (typically 5–10 mM whole blood [lactate] at the end of exercise) (Pringle and Jones, 2002). When blood [lactate] is stable over time (even if it is elevated above resting values), it has been suggested that there is no net contribution of anaerobic ATP production to total ATP turnover (Antonutto and di Prampero, 1995). The CP might therefore also be considered to represent the work rate above which anaerobic ATP production makes an increasingly important contribution to energy metabolism.

In contrast to the clear differentiation between the V̇O2 dynamics in the various domains of ‘sub-maximal’ exercise, much less is known about the V̇O2 response to constant-load exercise when the work rate approaches or exceeds that corresponding to V̇O2 peak (as measured, for example, during a ramp exercise test) (e.g. Hughson et al., 2000, Scheuermann and Barstow, 2003). At ‘extreme’ work rates (Hill et al., 2002), the exercise duration (typically 1–3 min at 105–120% V̇O2 peak) is so short that a V̇O2 slow component can be difficult to discern and the overall kinetics (following Phase I) can be adequately described with a single exponential term (Hill and Stevens, 2001, Ozyener et al., 2001). Naturally, for extreme exercise with a V̇O2 requirement > V̇O2 peak, the gain of the V̇O2 response at the end of exhaustive exercise will fall below ∼10 ml min−1 W−1 because the increase in V̇O2 towards the V̇O2 requirement, as reflected by the muscle ATP turnover rate, will be constrained by the attainment of V̇O2 peak (or fatigue even before V̇O2 peak is reached). However, it has been argued by Whipp (1994) that, at the onset of extreme exercise, V̇O2 should initially project toward the ‘steady state’ V̇O2 requirement for the imposed work rate such that the gain of the asymptote of the modelled Phase II V̇O2 response (Gp) should approximate 10 ml min−1 W−1, provided that the fit is not contaminated by a ‘plateauing’ of V̇O2 as the peak is approached.

However, several recent studies have reported that Gp is significantly lower for high-intensity cycle exercise compared to moderate intensity cycle exercise (Jones et al., 2002; Pringle et al., 2003a, Pringle et al., 2003b; Scheuermann and Barstow, 2003). It is possible that the fall in Gp occurs when the work rate exceeds the CP (i.e. where the anaerobic contribution to energy metabolism becomes progressively more important) although this has not been directly investigated. However, because the Gp appears to fall below the anticipated ∼10 ml min−1 W−1 even during ostensibly ‘sub-maximal’ exercise in which there is sufficient time for a true steady state V̇O2 to be achieved, this also draws into question the assumption that V̇O2 will project towards the actual ‘steady state’ V̇O2 requirement during extreme exercise. Indeed, Scheuermann and Barstow (2003) have recently reported that Gp fell progressively at higher work rates within the extreme exercise intensity domain. However, these authors did not determine whether the fall in the Gp that they observed for extreme exercise was, in part, the result of including the plateau of V̇O2 as it approached its peak. In this respect, fitting only the early portion (i.e. first 45–60 s) of Phase II response would have been of interest. Furthermore, the participants in the study of Scheuermann and Barstow (2003) only performed one transition to the extreme work rates. It is known that the V̇O2 response to extreme exercise can be highly variable due in part to the reduced number of data points when exercise intensity is high and time to fatigue is correspondingly short (Özyener et al., 2001). Reducing breath-to-breath noise by averaging together the V̇O2 responses to a number of repeat transitions is necessary to more clearly unveil the V̇O2 response dynamics (Lamarra et al., 1987).

The purpose of the present study was therefore to re-examine the dynamics of the V̇O2 response to high-intensity (severe and extreme) exercise, and to compare these responses to the V̇O2 kinetics observed within the moderate and heavy exercise domains using the averaged response to a sufficient number of transitions to increase confidence in the modelled parameters. Our principal focus was on the influence of exercise intensity on the gain of the fundamental component of the V̇O2 response. Our first hypothesis was that Gp would fall substantially only when the work rate exceeded the CP and blood [lactate] increased appreciably, i.e. when anaerobic metabolism makes an increasingly important contribution to energy metabolism (Antonutto and di Prampero, 1995). Our second hypothesis was that Gp would be significantly lower for extreme exercise compared to moderate exercise both when the data were modelled to the end of exercise and when only the first 45 s of Phase II data were modelled.

Section snippets

Participants

Seven healthy males (mean ± S.D. age 24.7 ± 3.0 years, body mass 76.6 ± 8.8 kg) volunteered to participate in this study that had received approval from the Manchester Metropolitan University Research Ethics Committee. The participants gave written informed consent after the benefits and risks of taking part in the study were fully explained to them. The participants were all recreationally active and were fully familiar with laboratory testing procedures. On test days, the participants were

Results

The participants’ V̇O2 peak as measured during the ramp test was 50.0 ± 1.7 ml kg−1 min−1 with the GET occurring at 51 ± 4% V̇O2 peak. The mean work rate applied at each of the exercise intensities along with the some of the physiological responses measured at the end of exercise are shown in Table 1. The CP occurred at 280 ± 8 W or ∼57% Δ. Therefore, we were successful in having our participants perform one work rate between the GET and CP (i.e. at 40% Δ; heavy exercise) and one work rate between

Discussion

Consistent with our hypothesis, we found that the Gp fell significantly below the value seen for moderate exercise (∼9.7 ml min−1 W−1) only when the work rate exceeded the CP. Our results therefore confirm recent reports that the Gp is significantly lower during high-intensity compared to moderate intensity cycle exercise (Jones et al., 2002; Pringle et al., 2003a, Pringle et al., 2003b) and extend these observations by demonstrating that the Gp only fails to attain the anticipated value during

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